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Cell bioprinting technologies aim to fabricate tissue-like constructs by delivering biomaterials layer-by-layer. Bioprinted constructs can reduce the use of animals in drug development and hold promise for addressing the shortage of organs for transplants. We recently introduced a laser-assisted drop-on-demand bioprinting technology termed Laser Induced Side Transfer (LIST). This technology can print delicate cell types, including primary neurons. This bioprinting protocol includes the following key steps: cell harvesting, bio-ink preparation, laser setup priming, printing, and post-printing analysis. This protocol includes a detailed description of the laser setup, which is a rather unusual setup for a biology lab. This should allow easy reproduction by readers with basic knowledge of optics. Although we have focused on neuron bioprinting, interested readers will be able to adapt the protocol to bioprint virtually any cell type.
Learn More >Chronic pain results from a complex series of biomechanical, inflammatory, neurological, psychological, social, and environmental mechanisms. Pain and pain-related diseases are the leading causes of disability and disease burden globally. Employing nature-based interventions for the treatment of pain is an emerging field. Current theory driving the suggested mechanism(s) linking the pain reducing effects of nature-based interventions is lacking. A two-step approach was taken to complete a theoretical review and analysis. First, a literature review was completed to gather a substantive amount of research related to theoretical frameworks on the topic of nature-based interventions and pain. Secondly, a theoretical analysis as proposed by Walker and Avant was completed to explore current theoretical frameworks accepted in the literature on nature-based interventions and pain. Stress reduction theory and attention restoration theory were the most common theoretical frameworks identified. Neither theoretical framework explicitly identifies, describes, or intends to adequately measure the concept of pain, revealing a limitation for their application in research with nature-based interventions and pain. Theoretical development is needed, as it pertains to nature-based interventions and pain. Without this development, research on nature-based interventions and pain will continue to use proxy concepts for measurement and may result in misrepresented findings.
Learn More >Graves' disease has been reported to affect the clinical features of moyamoya disease (MMD), an occlusion of the circle of Willis. This study aimed to clarify the characteristics of MMD in patients with Graves' disease. This was a single-center, retrospective study. The prevalence and clinical features of MMD patients among all patients with thyroid disease who visited Ito hospital from January 2005 to December 2019 were evaluated. The relationship between MMD and hyperthyroidism was analyzed in new-onset Graves' disease patients during the same period. Of all 394,422 patients with thyroid disease, 88,180 had Graves' disease, and 40 had MMD with Graves' disease, i.e., the prevalence was 45.36 per 100,000 patients with Graves' disease (0.0454%). The median age at onset of MMD was 39 years (interquartile range, 31-54 years), with a male to female ratio of 1:12. The most common time that MMD was diagnosed was within 1 year after the onset of Graves' disease, in 9 of 40 patients (22.5%), and 19 of 40 patients (47.5%) underwent bypass surgery for MMD. In MMD with Graves' disease, headache was the most frequent symptom, and ischemic types of stroke and bilateral lesions were common. Of 23,347 patients with new-onset Graves' disease, 7 were diagnosed with MMD and the incidence of MMD was 5.94 patients per 100,000 person-years. Most patients developed MMD symptoms during hyperthyroidism. Although MMD is a rare condition, it should be noted that it can occur with Graves' disease.
Learn More >Different hypotheses have been proposed about the role of lumbar connective tissue in low back pain (LBP). However, none of the previous studies have examined the change in the elastic behavior of lumbar fascia in patients with LBP. The present study aimed to evaluate the changes in the elastic behavior of lumbar fascia in patients with chronic non-specific LBP based on ultrasound imaging.
Learn More >Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a challenging entity with complicated symptoms for treatment in the male crowd. Accumulating evidence revealed the dysfunction in the central system should be a critical factor for the pathogenesis and development in the CP/CPPS. Therefore, we recruited 20 patients of CP/CPPS and 20 healthy male volunteers, aged 20 to 50 years. Through resting-state functional magnetic resonance imaging (fMRI), we analyzed the mean amplitude of low-frequency fluctuations (mALFF) and the mean fractional amplitude of low-frequency fluctuations (mfALFF) to reflect the spontaneous abnormal activated regions in the brains of CP/CPPS patients. Compared to the healthy controls, the group with CP/CPPS had significantly increased mALFF values in the thalamus and augmented fALFF values in the inferior parietal lobule and cingulate gyrus. Significant positive correlations were observed in the extracted mALFF values in the midbrain periaqueductal gray matter (PAG) and the pain intensity ( = 0.2712, = 0.0019), mALFF values in the thalamus and the scores of Hospital Anxiety and Depression Scale (HADS) anxiety subscale ( = 0.08477, = 0.0461), and mfALFF values in the superior frontal gyrus (SFG) and the scores of the HADS anxiety subscale ( = 0.07102, = 0.0282). Therefore, we delineated the clinical alterations in patients of CP/CPPS that might be attributed to the functional abnormality of the thalamus, inferior parietal lobule, and cingulate gyrus. Among these regions, the PAG, thalamus, and SFG may further play an important role in the pathogenesis, with their regulating effect on pain or emotion.
Learn More >Central sensitization caused by spinal disinhibition is a key mechanism of mechanical allodynia in neuropathic pain. However, the molecular mechanisms underlying spinal disinhibition after nerve injury remain unclear. Here, we show in mice that spared nerve injury (SNI), which induces mechanical hypersensitivity and neuropathic pain, triggers homeostatic reduction of inhibitory outputs from dorsal horn parvalbumin-positive (PV+) interneurons onto both primary afferent terminals and excitatory interneurons. The reduction in inhibitory outputs drives hyperactivation of the spinal cord nociceptive pathway, causing mechanical hypersensitivity. We identified the retinoic acid receptor RARα, a central regulator of homeostatic plasticity, as the key molecular mediator for this synaptic disinhibition. Deletion of RARα in spinal PV+ neurons or application of an RARα antagonist in the spinal cord prevented the development of SNI-induced mechanical hypersensitivity. Our results identify RARα as a crucial molecular effector for neuropathic pain and a potential target for its treatment.
Learn More >Neuropathic pain in neuromyelitis optica spectrum disorder (NMOSD) is common but has always been overlooked. This study was conducted to explore factors correlated with neuropathic pain in NMOSD and to evaluate associations between pain and quality of life.
Learn More >Despite being a first-line treatment recommendation, there is uncertainly for how exercise helps people with chronic low back pain. We designed this study to examine how exercise might help people with chronic low back pain by following a large community sample for 1-year. Qualitative questionnaires and self-report measures were collected every 3-months for 1-year in 400 people with chronic low back pain. People were not provided any specific treatment advice as part of this study but were allowed to engage with any normal physical activity, treatment, or medication as part of their normal life. Exercise engagement was defined from inspection of participant qualitative responses, according to minimum acceptable levels of exercise that elicit symptom reduction. Multiple mediation analysis was performed to examine the effect of exercise engagement on disability through the proposed mediators (pain, fear, catastrophizing, depression, anxiety, self-efficacy). The significant effect of exercise engagement on reductions in disability at 6- and 12-months was explained through pain and catastrophizing. People with chronic low back pain who reported worsening of symptoms over the year had similar reporting of exercise throughout the 12-months to people who had improvements in disability. Exercise can reduce disability through the effect on pain and catastrophizing, but how this effect occurs (i.e., an active or passive component of exercise) is unclear.
Learn More >Contagious itch behavior informs conspecifics of adverse environment and is crucial for the survival of social animals. Gastrin-releasing peptide (GRP) and its receptor (GRPR) in the suprachiasmatic nucleus (SCN) of the hypothalamus mediates contagious itch behavior in mice. Here, we show that intrinsically photosensitive retina ganglion cells (ipRGCs) convey visual itch information, independently of melanopsin, from the retina to GRP neurons via PACAP-PAC1R signaling. Moreover, GRPR neurons relay itch information to the paraventricular nucleus of the thalamus (PVT). Surprisingly, neither the visual cortex nor superior colliculus is involved in contagious itch. In vivo calcium imaging and extracellular recordings reveal contagious itch-specific neural dynamics of GRPR neurons. Thus, we propose that the retina-ipRGC-SCN-PVT pathway constitutes a previously unknown visual pathway that probably evolved for motion vision that encodes salient environmental cues and enables animals to imitate behaviors of conspecifics as an anticipatory mechanism to cope with adverse conditions.
Learn More >Neuropathic pain is still a challenge for clinical treatment as a result of the comprehensive pathogenesis. Although emerging evidence demonstrates the pivotal role of glial cells in regulating neuropathic pain, the role of Schwann cells and their underlying mechanisms still need to be uncovered. Pannexin 1 (Panx 1), an important membrane channel for the release of ATP and inflammatory cytokines, as well as its activation in central glial cells, contributes to pain development. Here, we hypothesized that Schwann cell Panx 1 participates in the regulation of neuroinflammation and contributes to neuropathic pain.
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